from Section 2 - Psychophysiological processes in disease
Published online by Cambridge University Press: 05 August 2016
Abstract
Socially stressed adult male cynomolgus monkeys (Macaca fasdcularis) fed a low fat, low cholesterol diet developed more extensive coronary artery atherosclerosis than unstressed controls. Groups did not differ in serum lipids, blood pressure, serum glucose, or ponderosity. These results suggest that psychosocial factors may influence atherogenesis in the absence of elevated serum lipids. Psychosocial factors thus may help explain the presence of coronary artery disease (occasionally severe) in people with low or normal serum lipids and normal values for the other “traditional” risk factors.
The initiation and progression of coronary artery atherosclerosis is often associated with increased concentrations of lipids in the serum (1). Despite this association, many individuals develop severe atherosclerotic lesions while having low serum lipid concentrations, and others develop far more atherosclerosis than would be expected on the basis of a modest evaluation of serum lipids (2). Work with animal models suggests that some of this variability may be explained by the influence of hypertension and immunologic injury to arteries, (3, 4). Yet, much additional variability in atherosclerosis lesion extent remains unexplained, suggesting the existence of other pathogenic mechanisms among normocholesterolemic individuals. In recent years, psychosocial variables have been linked increasingly to ischemic heart disease in human beings (5) and psychosocial manipulations have been shown to exacerbate atherosclerosis in cholesterol-fed cynomolgus monkeys, rabbits, and swine (6-8). At present, though, it is unclear whether psychosocial manipulations are capable of promoting atherogenesis in normocholesterolemic animals and, by implication, in human beings with low or normal serum cholesterol concentrations. The purpose of the present investigation was to provide an initial test of this hypothesis. Our results demonstrate that socially stressed monkeys fed a low fat, low cholesterol diet developed more extensive intimal lesions in the coronary arteries than control animals living under unstressed conditions. Moreover, the differences in lesion extent observed here were not associated with elevations or group differences in serum lipids, blood pressure, serum glucose, or ponderosity.
The experimental animals were 30 male, cynomolgus monkeys (Macaca fascicularis), imported as adults from Malaysia and the Philippine Islands. They were assigned to two experimental conditions (designated the “stressed” and “unstressed” conditions), and within each condition (N = 15), the monkeys were divided randomly into three, five-member groups. During the study, all groups were housed separately in identical pens measuring 2.0 by 3.2 by 2.5 m.
To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Find out more about the Kindle Personal Document Service.
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.